胰腺疾病相关性门脉高压症59例临床分析

目的探讨胰腺疾病相关性门脉高压症的临床特点及治疗。方法选择我院1986年1月至2005年4月收治的胰腺疾病相关性门脉高压症患者，回顾性分析其一般资料、受累静脉、临床表现、实验室和影像检查、治疗和结局。结果我院19年共收治本病59例，占同期门脉高压症的4．0％。常见基础胰腺疾病依次为慢性胰腺炎（21例，35．6％）、胰腺癌（20例，33．9％）、急性胰腺炎（8例，13．6％）和胰腺囊肿（3例，5．1％）。40例患者有明确的受累静脉，其中脾静脉阻塞27例（67．5％）、门静脉阻塞16例（40．0％）。脾脏肿大48例（81．4％），为轻、中度肿大，脾功能亢进31例（52．5％），程度较轻，以白细胞减少为主。45例患者（76．3％）有胃、食管静脉曲张（孤立性胃静脉曲张35例），19例有破裂出血（32．2％）。药物治疗可控制急性出血，但不能预防再出血。18例行脾切除术，主要指征是反复发生的消化道出血，术后患者均未再出血（随访8个月～9年）。结论胰腺疾病可累及门静脉主干及其属枝，导致广泛性或区域性门脉高压症。药物治疗可有效控制急性曲张静脉破裂出血，而手术可能是防止再出血的主要措施。     

Portal vein resection without reconstruction during Appleby operation in a patient with pancreatic body carcinoma with cavernous transformation.

The prognosis of pancreatic body carcinoma has been poor due to cancerous invasion of major vessels. Resection of the involved vessels may improve resectability and prognosis. We report a patient who had a pancreatic body carcinoma with cavernous transformation of the portal vein, in whom the portal vein was resected without reconstruction during an Appleby operation. A 67 year-old man was admitted for evaluation of back pain. Enhanced computed tomography showed no main trunk of the portal vein but a developed collateral circulation. Celiac angiography revealed encasement of the common hepatic, splenic and celiac artery. Venous angiography revealed obstruction of the portal and splenic veins with cavernous transformation surrounding these veins. Pre-operative diagnosis was carcinoma in the pancreatic body, which invaded the portal vein, the celiac and common hepatic arteries. The Appleby operation combined with resection of the portal vein without reconstruction could be performed, by preserving collateral vessels and monitoring hepatic venous oxygen saturation (ShvO2) to prevent hepatic ischemia caused by occlusion of the portal vein. The post-operative course was uneventful.     

Cavernous transformation of the portal vein in nephrotic syndrome

We report a 19-year-old man with thrombosis of the portal vein associated with a nephrotic syndrome. A computed tomography showed obstruction of the portal vein with prominent collaterals and cavernous transformation. This case is noteworthy as a report of nephrotic syndrome accompanied by extensive abdominal venous thrombosis and was cured successfully.     

Cholestasis as presenting symptom of portal cavernoma

A 51-year-old man with a history of portal vein thrombosis, was examined because of elevated liver tests and a tumoral mass in the liver hilus. Computed tomography (CT) scan and magnetic resonance imaging confirmed the portal vein thrombosis and an infiltrating mass in the porta hepatis with compression on the common bile duct. Endoscopic retrograde cholangiography showed an irregular narrowing of the mid-part of the common bile duct. The patient was referred for explorative laparotomy, which revealed a hypervascular mass in the liver hilus surrounded by many blood vessels. The diagnosis of portal cavernoma was made. Further haematological examination for the cause of portal vein thrombosis revealed an anti-phospholipid syndrome as well as myeloproliferative disease. Oral anticoagulant treatment is started. In conclusion, we report a case of biliary stricture due to portal vein thrombosis and cavernoma (portal biliopathy) which was not diagnosed preoperatively. Biliary strictures associated with portal vein thrombosis are due to extrinsic compression by collaterals and can also be induced by ischemic injury secondary to venous and arterial thrombosis of the choledochal vascular plexus.     

Venous tumor thrombosis and cavernous transformation of the portal vein in a patient with gastric carcinoma

A case of extensive extra-and intrahepatic portal tumor thrombosis, with no metastatic foci in liver parenchyma, secondary to advanced gastric carcinoma in a 69-year-old man is reported. The portal tumor thrombosis was characterized by enlargement of the thrombosed segment of the vein, decreased density mass without intraluminal enhancement of the involved vein, nonvisualization of the portal venous branch in the involved lobe, and the so-called cavernous transformation of the portal vein. The surgically resected gastric specimen showed Borrmann type 3 advanced papillary adenocarcinoma. The portal tumor thrombus is presumed to have arisen from vascular invasion in the primary foci of gastric carcinoma, and then to have permeated the portal vein without invasion of liver parenchyma.     

Should anticoagulants be administered for portal vein thrombosis associated with acute pancreatitis?

Venous complications in patients with acute pancreatitis typically occur as a form of splenic, portal, or superior mesenteric vein thrombosis and have been detected more frequently in recent reports. Although a well-organized protocol for the treatment of venous thrombosis has not been established, anticoagulation therapy is commonly recommended. A 73-year-old man was diagnosed with acute progressive portal vein thrombosis associated with acute pancreatitis. After one month of anticoagulation therapy, the patient developed severe hematemesis. With endoscopy and an abdominal computed tomography scan, hemorrhages in the pancreatic pseudocyst, which was ruptured into the duodenal bulb, were confirmed. After conservative treatment, the patient was stabilized. While the rupture of a pseudocyst into the surrounding viscera is a well-known phenomenon, spontaneous rupture into the duodenum is rare. Moreover, no reports of upper gastrointestinal bleeding caused by pseudocyst rupture in patients under anticoagulation therapy for venous thrombosis associated with acute pancreatitis have been published. Herein, we report a unique case of massive upper gastrointestinal bleeding due to pancreatic pseudocyst rupture into the duodenum, which developed during anticoagulation therapy for portal vein thrombosis associated with acute pancreatitis.     

Portal vein thrombosis： Etiology and clinical outcome of cirrhosis and malignancy-related non-cirrhotic, non-tumoral extrahepatic portal venous obstruction

The etiology and pathogenesis of portal vein thrombosis are unclear. Portal venous thrombosis presentation differs in cirrhotic and tumor-related versus non-cirrhotic and non-tumoral extrahepatic portal venous obstruction (EHPVO). Non-cirrhotic and non-tumoral EHPVO patients are young and present with well tolerated bleeding.Cirrhosis and tumor-related portal vein thrombosis patients are older and have a grim prognosis. Among the 118 patients with portal vein thrombosis, 15.3% had cirrhosis, 42.4% had liver malignancy (primary or metastatic), 6% had pancreatitis (acute or chronic), 5% had hypercoagulable state and 31.3% had idiopathy,12% had hypercoagulable state in the EHPVO group.     

Splenic and portal venous obstruction in chronic pancreatitis

The aim of this study was a prospective search for splenoportal venous obstruction (SPVO) in a medical-surgical series of 266 patients with chronic pancreatitis who were followed up a mean time of 8.2 years. SPVO was systematically searched for using ultrasonography and then confirmed by angiography or computed tomography. SPVO was found in 35 patients (13.2%) but was symptomatic in only two. Initial obstruction involved the splenic vein in 22 patients, the portal vein in 10, and the superior mesenteric vein in three. Since venous obstruction extended from the splenic to the portal vein in five patients, the prevalence of portal obstruction was 5.6% (15/266). Acute pancreatitis and pseudocysts were the probable cause of SPVO in 91.4% of our cases. Half the cases of splenic venous obstruction were related to pseudocysts of the caudal pancreas. Esophageal varices were found in two patients and gastric varices in four at the time of diagnosis and during follow-up. At the end of follow-up, 12 patients had undergone splenopancreatectomy (N = 11) or splenectomy (N = 1). Only one patient was operated on for massive esophageal variceal bleeding, and another patient died due to intractable colic variceal bleeding. In four of six patients operated on with portal vein obstruction, surgery was difficult due to venous collaterals. Ten patients were not operated on and 13 patients operated on were not treated for SPVO. The mean follow-up after diagnosis of SPVO for these final 23 patients was 28.9 months. None of these patients bled.(ABSTRACT TRUNCATED AT 250 WORDS)     

胃底静脉曲张对诊断脾静脉血栓形成之意义

目的探讨胃底静脉曲张对诊断脾静脉血栓形成之意义?方法分析过去的23年里，在临床上遇见9例脾静脉血栓形成(SVT)的患者，皆有胃底静脉曲张(GFV)，外科手术后和利用静脉造影术观察脾静脉栓塞情况。结果选择性脾动脉造影(SSAG)和肠系膜上动脉造影(SMAG)静脉相期未显示脾静脉(SPV)，SSAG和经皮肝门静脉造影(PTP)又见胃短静脉和左胃网膜静脉显著扩张，然PTP影象较ssAc清晰，特别是GFV。5例外科和病理剖开SPV见到血栓形成。结论当内镜见有GFV，特别是IGFV如肯定除外IPH或肝硬化者，此GFV是诊断SVT的秘诀。对SVT单纯行脾切除术是可完全治愈的一种左侧门静脉高压；     

Mesenteric and portal vein thrombosis presenting as acute intestinal obstruction.

Acute bowel infarction is a major complication in patients with superior mesenteric vein and portal vein thrombosis. However, in some patients, sufficient collaterals can prevent acute bowel infraction. We present a case of mesenteric vein and portal vein thrombosis with intestinal obstruction due to acute bowel oedema and ischaemic adhesion without infarction or stenosis.     

Sinistral portal hypertension and distal splenorenal shunt during pancreatic surgery

Locally advanced pancreatic cancer located in the head or un-cinate process(i.e.,uncus)often invades the confluence of the superior mesenteric vein(SMV),portal vein(PV),and splenic vein(SV)[1,2].Additionally,chronic pancreatitis easily occludes drainage flow via the SV[3].These pancreatic diseases force sur-geons to perform en bloc resection of the SV.Simple ligation of the remnant SV without venous resection results in sinistral por-tal hypertension(PH)(i.e.,left-sided PH),gastrointestinal bleeding,splenic congestion,and hypersplenism over the long term[1,2].     

Sonographic demonstration of portal venous system thromboses secondary to inflammatory diseases of the pancreas

Sonographic demonstration of abdominal venous thromboses subsequent to pancreatic benign inflammatory diseases has been seldom reported up to now. Seven cases of thromboses of the portal venous system associated with acute or chronic pancreatitis are reported. All cases were detected by sonography in patients without clinical manifestations of portal hypertension. Echogenic thrombus within the lumen of the vein was observed only in the short-term follow-up of acute pancreatitis. Cavernomatous transformation was observed in 6 patients with long-term calcifying pancreatitis. Extrinsic compression by pseudocyst of the pancreas was observed in only 1 case. In all the other cases, thromboses seems to be secondary to local inflammatory phenomena during previous episodes of acute pancreatitis.     

Hepatic radionuclide angiography and Doppler ultrasonography in the detection and assessment of vascular disturbances in the portal system

BACKGROUND/AIMS: The aim of the study was evaluation of the morphology of the blood vessels, blood flow velocity and direction with Doppler ultrasound (D-US) and correlation with the relative liver parenchymal perfusion assessed by hepatic radionuclide angiography (HRA). METHODOLOGY: Real-time, D-US and HRA were performed in 108 patients. RESULTS: In patients with portal venous aneurysm, hepatopetal blood flow was increased, while portal perfusion did not differ from controls. In portal hypertensive patients, D-US detected dilatation of the portal system veins, with decreased blood flow. In comparison to the portal perfusion in controls and portal venous aneurysm, values were significantly (p < 0.01) lower in chronic active hepatitis and liver cirrhosis and differed between themselves (p < 0.01). In the groups of cirrhotic patients with esophageal varices, sclerosed esophageal varices, recanalized umbilical vein, partial portal thrombosis and cavernous portal vein with hepatofugal, hyperkinetic or slow blood flow, and very low velocities beside the thrombi, portal perfusion was lower (p < 0.01) than in controls, portal venous aneurysm, chronic active hepatitis and liver cirrhosis without collaterals. In complete thrombosis, minimal collateral flow was found with D-US, while HRA proved no portal supply. CONCLUSIONS: D-US and HRA are complementary for the estimation of various liver vascular disorders.     

慢性胰腺炎伴胰头部病变的外科手术处理

目的 探讨慢性胰腺炎伴胰头病变患者的外科处理。方法 回顾性总结分析了1998年10月至2001年12月收治27例慢性胰腺炎伴胰头病变患者的临床资料。其中：保留幽门的胰十二指肠切除（PPPI手术）14例（32例慢性胰腺炎的患者术前已有门静脉栓塞），保留十二指肠胰头切除（Beger手术）2例，胰头部分切除，胰空肠侧侧吻合（Frey手术）2例，胰十二指肠切除（Whipple手术）9例，结果 2例慢性胰腺炎合并门静脉血栓的患者术前先行门静脉取栓，降低门静脉压力，然后再针对慢性胰腺炎实行外科手术，术后1例恢复顺利，另1例死于多器官脏器功能衰竭，总的院内并发症率25%，总院内死亡率4%，其中PPPD手术后院内并发症率21%，院内死亡率7%。结论 慢性胰腺炎伴胰头肿大的患者的手术治疗应根据胰腺和邻近周围其它器官的形态学改变决定手术的方法。其结果不仅可以有效地治疗慢性胰腺炎，同时有助于提高胰头癌的诊治水平。     

Acute portal vein thrombosis due to chronic relapsing pancreatitis: a fistula between a pancreatic pseudocyst and the splenic vein

Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but several other causes might play an important role in PVT pathogenesis. We present a case of alcoholic chronic pancreatitis complicated by acute extensive PVT. The patient was managed conservatively with danaparoid sodium at first, but the thrombosis gradually extended. We then tried radiological intervention using the direct transhepatic and transjugular intrahepatic postsystemic shunt approaches. Although we were able to successfully catheterize the percutaneous transhepatic portal vein (PTP), we could not achieve recanalization of the portal vein. Therefore, PTP catheterization and systemic intravenous infusion of urokinase and heparin was performed to prevent further progression of the thrombosis and cavernous transformation was finally achieved. Computed tomography (CT) and magnetic resonance cholangiopancreatography revealed a pancreatic stone which had possibly induced dilatation of the tail duct and formation of a pancreatic pseudocyst and caused intractable pancreatitis. We performed endoscopic retrograde cholangiopancreatography and placed a stent in the pancreatic duct, which completely cured the pancreatitis. Retrospectively, the previous CT with curved multi-planar reconstruction was reviewed and a fistula was detected between the pancreatic pseudocyst and splenic vein. We concluded that the etiology of the PVT was not only inflammatory extension from pancreatitis but also a fistula between the pancreatic duct and the splenic vein.     

Portal vein thrombosis associated with hilar bile duct carcinoma and liver abscess

As most portal vein occlusion in hilar bile duct carcinoma is caused by tumor invasion to the portal vein, other mechanisms of its occlusion are very rare. We report the case of a 69-year-old man who underwent surgical resection for an advanced hilar bile duct carcinoma associated with unusual portal vein occlusion. Preoperative diagnosis was advanced hilar bile duct carcinoma with liver abscess and right portal vein occlusion due to tumor invasion. Extended right hepatectomy combined with resection of caudate lobe was performed. Intraoperatively, tumor invasion to the portal vein was not evident and resected margin of the right portal vein showed thrombosis and no evidence of malignancy histologically. To our knowledge, this is the first reported case of a patient with a combination of portal vein thrombosis and liver abscess in hilar bile duct carcinoma. Although portal vein occlusion due to thrombosis is an unusual complication in hilar bile duct carcinoma, the presence of liver abscess may be a useful diagnostic implication of this occlusion.     

Hepatic hemodynamics and functions in extrahepatic portal obstruction in the rat with liver cirrhosis

Portal vein obstruction due to a thrombus may be encountered in liver cirrhosis. However, the effect of portal vein obstruction on hepatic hemodynamics and functions, and on collateral formation has not been clear in liver cirrhosis. To rectify this, the cirrhotic rat model with portal vein ligation was evaluated. In addition to the early recovery of hepatic blood flow, the reduction in hepatic blood flow after portal vein ligation was less in the cirrhotic rat than in the normal rat. The portogram showed that, in addition to hepato-fugal collaterals, hepato-petal collaterals developed well and early in the cirrhotic rat as compared with the normal rat. Although mitochondrial functions before portal vein ligation deteriorated in the cirrhotic rat, the decrease after portal vein ligation was less, and the recovery of function was earlier in the cirrhotic than the normal rat. The influence of portal vein obstruction on hepatic hemodynamics and functions in the cirrhotic rat was less than in the normal rat, due to earlier and significant formation of hepato-petal collaterals.     

Sinistral portal hypertension. A case report

Sinistral portal hypertension is a clinical syndrome of gastric variceal hemorrhage in the setting of splenic vein thrombosis due to a primary pancreatic pathology. The distinguishing features from other forms of portal hypertension are preserved liver function and a patent extrahepatic portal vein. The important causes include acute and chronic pancreatitis, pancreatic pseudocysts and pancreatic carcinomas. Benign pancreatic neoplasms only rarely cause sinistral portal hypertension. Splenic vein thrombosis complicates 7-20% of patients having pancreatitis or a pancreatic pseudocyst; however, bleeding occurs in only approximately 5% of patients. The diagnosis of sinistral portal hypertension is achieved by a combination of gastroscopy, liver function tests, ultrasound examination (with Doppler) and/or contrast-enhanced CT scan of the abdomen. A mere demonstration of sinistral portal hypertension does not warrant intervention. An expectant management is justifiable in asymptomatic patients with pancreatitis. However, concomitant splenectomy may be considered in patients undergoing operative treatment of symptomatic chronic pancreatitis if sinistral portal hypertension and gastroesophageal varices are present. In patients presenting with gastric variceal hemorrhage, splenectomy (with treatment for the primary pancreatic pathology, e.g. distal pancreatectomy) is curative with excellent long term results.     

Portal and mesenteric vein and inferior vena cava thrombosis associated with antiphospholipid syndrome

We report a 48-year-old man with thrombosis of the portal and superior mesenteric vein and inferior vena cava associated with primary antiphospholipid syndrome (APS). Primary APS was diagnosed by a positive reaction with anticardiolipin antibody (aCL) and the absence of any evidence suggesting the presence of other disease states known to be associated with aCL. A coeliac angiography showed obstruction of the portal and superior mesenteric vein with prominent collaterals and cavernous transformation. Femoral vein angiography showed total obstruction of the external iliac vein and inferior vena cava, and dilation of the pelvic veins, with contrast medium in the lumbar vein. This case is noteworthy as a report of primary APS accompanied by extensive abdominal and pelvic venous thrombosis.     

Splenic Vein Thrombosis as a Consequence of Chronic Pancreatitis: A Study of Three Cases

Splenic vein obstruction was found in three patients with chronic pancreatitis. All had suffered epigastric pain, but no specific findings which suggested obstruction of the splenic vein were evident on physical or laboratory examinations. Enlarged pancreatic contour with calculi and pseudocyst formation were observed by CAT scan in all three cases. Gastric varices were found in two patients who had episodes of gastric bleeding. The splenic vein was shown to be occluded in two patients in the venous phase of celiac angiography and was entirely nonvisualized by percutaneous portography in the third case. The first patient underwent elective surgery, while the second patient had emergency surgery due to intraabdominal abscess formation with gastric bleeding. The surgical procedure in both patients was splenectomy coupled with distal pancreatectomy. Thrombus formation was confirmed by venous dissection at surgery.